Management of behavioural and psychological symptoms of dementia

With the steady rise in numbers
of the world’s elderly population, the behavioural and
psychological symptoms of dementia (BPSD) have become increasingly
relevant to both
clinicians and families.

Carla Patricia Freeman, MB ChB, FCPsych (SA)

Department of Psychiatry and Mental Health, University of Cape Town

Carla
Freeman is a psychiatrist currently sub-specialising in the field of
neuropsychiatry at the Department of Psychiatry and Mental Health,
University of Cape Town. Her areas of interest include substance abuse
in the context of HIV infection and old-age psychiatry.

John Joska, FCPsych (SA), PhD

Associate Professor and Head of Division of Neuropsychiatry, Department of Psychiatry and Mental Health, University of Cape Town

John Joska is programme manager for HIV psychiatry and Cape Town Metro West old-age psychiatry.

Correspondence to:Carla Freeman (Carla.freeman@uct.ac.za)

Approximately 35 million people worldwide have dementia and this number is predicted to increase to 115 million by 2050.1 Behavioural
and psychological symptoms of dementia (BPSD) are a common complication
of dementia and between 70% and 90% of people with dementia will
experience BPSD at some point during their illness. BPSD results in
significantly greater caregiver burden, higher health-related economic
costs, poor quality of life and premature placement in nursing homes.2
The presence of BPSD has also been associated with disease progression
and greater cognitive decline in Alzheimer’s dementia (AD).3
Recognition of BPSD by the healthcare provider forms a central
component of the management of patients with dementia syndromes. This
article aims to provide clinicians with an overview of BPSD and an
approach to management, incorporating both non-pharmacological and
pharmacological strategies.

Behavioural and psychological symptoms of dementia

Cognitive impairment is a central feature of
dementia. However, multiple brain processes are disrupted as part of
the disorder, leading to a range of neuropsychiatric symptoms.
Neuropsychiatric symptoms in people living with dementia are often
referred to as BPSD, as they incorporate symptoms of disturbed
perception, thought content, mood or behaviour.4 These symptoms are listed in Table 1.

Patients may experience varying symptoms, or
combinations thereof, depending on the underlying cause or stage of
illness. Patients with more severe dementia (roughly correlating with
lower Mini Mental State Exam (MMSE) scores) are at increased risk for
psychosis, agitation and behavioural disturbance.5 The type of symptom may also assist with the diagnosis, e.g. visual hallucinations are frequently seen in Lewy Body dementia.

Aetiology of BPSD

By definition, BPSD occurs in the context of
dementia, and may be the direct result of the disorder, or aggravated
by additional factors. These include biological (e.g. pain, systemic
infection, dehydration, electrolyte disturbance, constipation),
psychological (e.g. exaggeration of pre-morbid personality traits,
grief due to multiple losses, depression) and environmental (e.g.
change of caregiver) components. Language impairment and disrupted
thought processes may render the patient unable to communicate the
cause of their distress, subsequently leading to behavioural
disturbance.

Making a diagnosis of BPSD

Clinicians managing patients with BPSD should
seek to confirm the type and severity of dementia present. This will
include collateral, bedside cognitive evaluation and appropriate
special investigations. When making the diagnosis of BPSD, limitations
in communication with the patient result in clinicians relying heavily
on reports from family members and caregivers. Clinical syndromes that
do not result in gross behavioural disturbance, e.g. depression, are
frequently under-reported, leading to under-diagnosis and a missed
opportunity for treatment. A number of clinical measures, specific to
dementia, have been designed to aid in the diagnosis of BPSD. These
measures provide a useful guide to a range of potential BPSD, their
severity, impact on caregivers, and allow the clinician to monitor
treatment efficacy in collaboration with the patient’s family.
These measures include: the neuropsychiatric inventory; the
behavioural pathology in Alzheimer’s disease rating scale;
Cornell scale for depression and the Cohen-Mansfield agitation
inventory.6
Families should be encouraged to record a 24-hour behaviour chart over
a few days to identify potential precipitants or problematic time
periods, e.g. bath time. Once a diagnosis has been made, the target
symptom, its duration, possible underlying cause and treatment strategy
should be communicated to the patient and caregiver.

Management of BPSD

Paramount to the management of BPSD is the
recognition of any underlying contributing physical illness (such as
delirium), psychological issues or environmental change. Features
suggestive of delirium include acute onset, confusion, fluctuation of
mental state, sun-downing and evidence of a systemic disturbance.
Drug-induced delirium, e.g. anticholinergics, antihypertensives and
antipsychotics, should always be considered in the differential
diagnosis and management of BPSD.

Few longitudinal studies of BPSD exist. Some
studies suggest that many symptoms remit spontaneously after a few
months. However, agitation, aggression, severe depression and psychosis
are less likely to resolve without treatment and require active
management.10

Non-pharmacological management strategies

Non-pharmacological management is considered first
line in the management of BPSD and should be employed regardless of
whether a decision is taken to commence medication. Routine monitoring
and evaluation need to be undertaken on a regular basis by the
clinician. These strategies are listed in Table 2.

Pharmacological treatment of BPSD

A modest number of individuals with dementia
may require pharmacotherapy for the treatment of BPSD. Antipsychotics
have traditionally been the treatment of choice for the management of
behavioural disturbance in dementia. Due to the recent Food and Drug
Administration (FDA) warnings of the increased risk of stroke in
elderly patients using all classes of antipsychotics and risk of
worsening confusion in dementia, these drugs are now considered second
line.11 A
useful approach when deciding on an appropriate agent would be to first
identify and treat depression and anxiety disorders if present,
secondly to consider cognitive enhancers where appropriate, and finally
consider alternative agents, e.g. anticonvulsants and antipsychotics.
When prescribing, consider the principles listed in Table 3.

Depression

Untreated depression increases mortality,
exacerbates cognitive and functional decline, impairs quality of life
and increases caregiver burden. Between 30% and 50% of patients with
dementia have depressive symptoms. Selective serotonin reuptake
inhibitors (SSRIs), e.g. citalopram and sertraline, are widely
available and are favoured as the treatment of choice in dementia with
co-morbid depression. Tricyclic antidepressants (TCAs), e.g.
amitriptyline, may be considered as second line, although the
anticholinergic, antihistaminic and cardiotoxic side-effects are
problematic in this population.12 Treatment response may be longer than that seen in adult populations.

Anxiety

Anxiety symptoms, e.g. anticipatory anxiety, may be
disabling and place additional strain on caregivers. Anxiety symptoms
are prominent in vascular dementia, frontotemporal dementia, and
dementia associated with Parkinson’s disease, when compared with
Alzheimer’s disease. A high co-morbidity exists between anxiety
and depression and both conditions should be addressed. Limited
guidelines exist for the treatment of anxiety in dementia. However,
most clinicians recommend the use of antidepressants to treat anxiety
symptoms. Benzodiazepines are relatively contraindicated due to their
cognitive side-effects, risk of respiratory depression in elderly
patients with chronic obstructive airway disease (COAD), increased risk
of falls and capacity for physical dependence.13

Psychosis

Antipsychotics are indicated for the
treatment of intrusive delusions and hallucinations associated with
dementia. Each antipsychotic confers its own risk versus benefit
profile and the choice of agent should be made according to the needs
of the individual patient. Typical, or first-generation antipsychotics
(FGAs), increase the risk of developing extra-pyramidal side-effects
(EPSEs), i.e. parkinsonism, acute dystonia, akathisia and tardive
dyskinesia. Atypical, or second-generation antipsychotics (SGAs), may
cause dyslipidaemias, impaired glucose tolerance and weight gain
leading to a metabolic syndrome.14
A risk-benefit analysis should be undertaken in every patient, taking
into account both medical co-morbidities and propensity to develop
disabling side-effects. Treatment is not recommended for periods longer
than 3 months. However, in more severe cases treatment may be required
for a longer duration.

Sleep disturbance

Sleep disturbance is common in dementia and may be
associated with or form part of BPSD. Patients with AD may experience
day-night reversal and those with Lewy Body dementia are at increased
risk of REM sleep disorders. Co-morbid medical conditions, e.g.
electrolyte disturbance, dehydration and infection, must be excluded as
possible causative factors. Medications known to disrupt sleep should
be evaluated.

Caregivers are often surprised when informed of the
physiologically decreased need for sleep associated with normal ageing.
Psycho-education forms part of management with regard to sleep hygiene
and the importance of a daily routine. Naps during the day should be
strongly discouraged. Some evidence exists for the use of
antidepressants, e.g. SSRIs and trazodone, to address sleep disturbance
in dementia. Non-benzodiazepine hypnotics, e.g. zolpidem, may be
considered as a short-term measure. Tolerance and dependence may occur
with these sedatives and caution is needed when co-prescribing
additional central nervous system depressants. The use of
benzodiazepines for sleep disturbance in dementia is not advised.

Agitation and aggression

Agitation and aggression form part of the BPSD
spectrum and occur in up to 50% of patients with advanced dementia. No
universally agreed upon definition for agitation exists and the term
includes a range of problem behaviours from wandering to frank
aggression. As mentioned previously, exclusion of an underlying medical
cause, including delirium, is essential to management. Clinicians and
family should adopt an empathic, non-punitive, person-centred approach
to managing the behaviour. Non-pharmacological management strategies
are a core component of treatment. A number of pharmacological options
are available for cases of severe behavioural disturbance. These are
discussed below.

In cases of mild to moderate AD, the
cholinesterase inhibitors (CHEIs) have had some success in improving
behaviour. Three agents – donepezil, galantamine and rivastigmine
– are available. These agents have similar efficacy data although
side-effects vary from person to person. A second agent should be
attempted if the first is intolerable. Memantine is an N-methyl-D-aspartate
(NMDA) receptor antagonist approved for moderate to severe AD. Positive
behavioural change in cases of vascular dementia and AD have been
reported.

Anticonvulsants, e.g. sodium valproate and
carbamazepine, may be considered in severe cases of behavioural
disturbance in all dementias. Drug-drug interactions between
anticonvulsants (mostly metabolised by the liver) and concurrent
medications may be problematic. As a second-line option, antipsychotics
have a place in the management of severe agitation associated with
dementia.15 No antipsychotic
is licensed for the treatment of dementia and is thus prescribed
off-licence. Families should provide informed consent and referral to a
psychiatrist is indicated in treatment-refractory cases.

Conclusion

The BPSD are common and cause significant distress
among patients and caregivers. A number of effective
non-pharmacological and pharmacological treatment options are available
to clinicians in the management of BPSD.

Declarations of interest

Carla Freeman is a 2010 recipient of a Discovery Foundation Academic Award.